Professional Documents
Culture Documents
Part I
Hassan Mohammad AlShehri
Intoduction
The bonding between gp120 and gp41 is only loose and therefore
gp120 may be shed spontaneously within the local environment.
virus
antibody
CD4 cells
25
HIV and AIDS
HIV Pathogenesis
The profound immunosuppression seen in AIDS is due to the
depletion of T4 helper lymphocytes.
In the immediate period following exposure, HIV is present at a high
level in the blood (as detected by HIV Antigen and HIV-RNA assays).
It then settles down to a certain low level (set-point) during the
incubation period. During the incubation period, there is a massive
turnover of CD4 cells, whereby CD4 cells killed by HIV are replaced
efficiently.
Eventually, the immune system succumbs and AIDS develop when
killed CD4 cells can no longer be replaced (witnessed by high HIV-
RNA, HIV-antigen, and low CD4 counts).
Acute Viral Syndrome
The natural history described in the following refers to HIV infection
in the absence of HAART.
Defined as the time period from initial infection with HIV to the
development of an antibody response.
Shows symptoms that often resemble those of mononucleosis. These
appear within usually 2 - 12 weeks following exposure to HIV.
However, clinical signs and symptoms may not occur in all patients.
There is usually a high plasma viremia and frequently a marked
decrease in CD4+ T-cells. The CD4+ T-cell count later increases
again, normally to levels inferior to the pre-infection values
Latency Period
Term .latency period. may be misleading, given the incredibly high
turnover of the virus and the relentless daily destruction of CD4+ T-
cells.
At the end of the latency period, a number of symptoms or illnesses
may appear which do not fulfil the definition of AIDS
Include slight immunological, dermatological, hematological and
neurological signs. Many of them are listed in the Category B of the
CDC classification system.
Constitutional symptoms, such as fever, weight loss, night sweats, and
diarrhea may also develop. In this situation, the level of 200 CD4+ T-
cells/µl is an important cut-off, below which the risk of many AIDS-
defining illnesses increases
latency may last 8-10 years or more.
HIV and AIDS
33
HIV and AIDS
34
Diagnosis
Laboratory Diagnosis
Serology is the usual method for diagnosing HIV infection. Serological
tests can be divided into screening and confirmatory assays. Screening
assays should be as sensitive whereas confirmatory assays should be as
specific as possible.
Screening assays - ELISA is the most frequently used screening assays.
The sensitivity and specificity of the presently available commercial
systems now approaches 100% but false positive and negative reactions
occur. Some assays have problems in detecting HIV-1 subtype O.
Confirmatory assays - Western blot is regarded as the gold standard for
serological diagnosis. However, its sensitivity is lower than screening
EIAs.
ELISA
False-positive results can occur with:
Antibodies to class II antigens
Autoantibodies
Hepatic disease
Recent influenza vaccination
Acute viral infections
ELISA
Western Blot
Most commonly used confirmatory test
Detects antibodies to HIV antigens of
specific molecular weights
Antibodies to HIV begin to appear within 2
weeks of infection.
Period of time between initial infection and
development of detectable antibodies is
rarely >3 months.
Western blot for HIV antibody
PCR
Rapid Tests
Rapid tests are similar to the standard
ELISA test in that they look for antibodies to
HIV in the patient’s blood+/-saliva+/-serum.
They are called “rapid” because the results
are available within an hour or less.
Reading Results: Genie II
Non-reactive Reactive
Reading Results: Determine
Non- Reactive
Reactive
Reactive
Reactive
Non-
Reactive
References
http://www.cdc.gov/hiv/resources/reports/hiv_prev_us.htm
http://www.cdc.gov/nchhstp/newsroom/docs/FastFacts-MSM-
FINAL508COMP.pdf
http://www.co.sanmateo.ca.us/vgn/images/portal/cit_609/31/5/1021425659
factors_delayed_hiv_article.pdf
Kumar and Clark Clinical Medicine
Harrison principle of internal medicine
Harrison's Principle of Internal Medicine
plaza.ufl.edu/mounaht/Group%25209%2520Chapter
%252030%2520Lesson%25202%2520Powerpoint(new)
%255B1%255D.ppt
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